ATP
(Synonyms: 腺苷三磷酸; Adenosine 5'-triphosphate) 目录号 : GC35420
ATP是代谢反应中底物激活的磷酸基供体，用于生物合成细胞内第二信使环状腺苷酸单磷酸（cAMP），并作为真正的细胞外信使介导细胞间通讯。
Cas No.:56-65-5
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
Characterization of ATP-gated P2×7 receptor functionality in colon cancer cell lines. (A,B): LOVO and SW480 cells were treated with ATP (0 mM), ATP (300 mM), BzATP (10 mM), ATP + A438079 (10 mM) or ATP + AZD9056 (10 mM), inward current of electrophysiological recording.
Agonists ATP(100–300 mM) (GLPBIO) or BzATP (10, 50, and 100 mM) were externally applied using a micromanipulator fast-flow delivery system for 10 s.
Front Cell Dev Biol 8 (2020): 1352. PMID: 33330466 IF: 6.6800 -
Related Biological Data
Extracellular ATP activated P2Y2 and increased Src and EGFR phosphorylation. (E−H) ATP activates Src and EGFR kinases in CAL27 (A and C) and SCC15 cells in a time-and dose-dependent manner.
The cells were treated with 100 μM ATP(GLPBIO) cultured with α-DMEMF12 for 14 days, and when they grew into a colony of 50 cells, the cells were washed with PBS and fixed with 4% methanol.
ACS omega 7.44 (2022): 39760-39771. PMID: 36385800 IF: 4.0998 -
Related Biological Data
The ATP-dependent activation of Leu527Phe variant.(A) Guanylyl cyclase activity was determined in HEK293T cells (expressing wild-type or Leu-527Phe variant of NPR2 or both) in the absence or presence of ATP (1–1000 μM) and 100nM CNP (n = 3).
The cells were pretreated with 0.1mM 3-isobutyl-1-methylxanthine (GLPBIO, Cat#GC11730,USA) for 15 min and then exposed to 100nM CNP (GLPBIO,Cat#GC43328, USA) and different concentrations of ATP (0 ~ 1000nM) (GLPBIO, Cat#GC35420, USA) for another 15 min.
Orphanet J Rare Dis 18.1 (2023): 221. PMID: 37501190 IF: 3.7001
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| Cell experiment [1]: | |
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Cell lines |
stem cells from human exfoliated deciduous teeth (SHEDs) |
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Preparation Method |
This study investigated the effects of extracellular ATP at a low (0.1 µM) and high (10 µM) concentration on the stemness and osteogenic differentiation of SHEDs. Cells were cultured in either growth medium or osteogenic medium with or without 0.1-10 µM ATP. |
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Reaction Conditions |
0.1-10 µM ATP; |
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Applications |
In growth medium, both concentrations of ATP increased the mRNA expression of pluripotent and osteogenic markers. In contrast, in osteogenic medium, 0.1 µM ATP enhanced in vitro mineralization, whereas 10 µM ATP inhibited this process. |
| Animal experiment [2]: | |
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Animal models |
rats |
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Preparation Method |
Subcutaneous injection of ATP induces pain-related behavior and hyperalgesia to mechanical and heat stimulation in rats. |
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Dosage form |
100 µM and 1 mM; s.c. |
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Applications |
ATP (100 µM and 1 mM, but not 1 µM) superfused for 5 min before the mechanical stimulation suppressed the mechanical responses of muscle thin fibers irrespective of whether they excited the fiber. |
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References: [1] Techatharatip O, et al. Biphasic Effect of ATP on In Vitro Mineralization of Dental Pulp Cells. J Cell Biochem. 2018 Jan;119(1):488-498. |
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ATP, as a phosphate-group donor for substrate activation in metabolic reactions, is required for the biosynthesis of the intracellular second messenger cyclic adenosine monophosphate (cAMP) and mediates intercellular communication as a bona fide extracellular messenger[1]. ATP can promote tumor progression or tumor suppression.[1].
In vitro, the IC50 value for ATP, α,β-meATP, and β,γ-meATP on these P2X receptors regulating IOP (intraocular pressure) was around 1.0 µM. P2X receptors present in the ciliary body are responsible for reducing IOP. Moreover, 1.0 µM ATP under light conditions causes a reduction in IOP of roughly 50% but when darkness occurs, ATP concentration is decreased to 0.30 µM, this concentration scarcely reducing IOP more than 16%[2]. There is a obvious increase in ECM (extracellular matrix) accumulation has been found in AF (annulus fibrosus) cells at a lower ATP treatment level (20 µM) compared with NP (nucleus pulposus) cells (100 µM), suugestng that AF cells are more sensitive to extracellular ATP than NP cells[3].
In vivo test it shown that Wistar rats were treated with 25 mg/kg ATP reduced bevacizumab-induced renal toxicity significantly more effectively than benidipine (4 mg/kg)[4]. Treatment with 1 and 5 mg/kg ATP intra-arterially (i.a.) close to the bladder in rats, produced rapid, phasic, dose-dependent increases in bladder pressure with micturition immediately after injection[5].
References:
[1]. Vultaggio-Poma V, et al. Extracellular ATP: A Feasible Target for Cancer Therapy. Cells. 2020 Nov 17;9(11):2496.
[2]. Pintor J. Light-induced ATP release from the lens. Purinergic Signal. 2018 Dec;14(4):499-504.
[3]. Gonzales S, et al. ATP promotes extracellular matrix biosynthesis of intervertebral disc cells. Cell Tissue Res. 2015 Feb;359(2):635-642.
[4]. Kocaturk H, et al. Effect of adenosine triphosphate, benidipine and their combinations on bevacizumab-induced kidney damage in rats. Adv Clin Exp Med. 2021 Nov;30(11):1175-1183.
[5]. Igawa Y, et al. Functional importance of cholinergic and purinergic neurotransmission for micturition contraction in the normal, unanaesthetized rat. Br J Pharmacol. 1993 Jun;109(2):473-9.
ATP是代谢反应中底物激活的磷酸基供体，用于生物合成细胞内第二信使环状腺苷酸单磷酸（cAMP），并作为真正的细胞外信使介导细胞间通讯。ATP可以促进肿瘤进展或抑制肿瘤。
在离体实验中，ATP、α,β-meATP和β,γ-meATP对调节眼压的这些P2X受体的IC50值约为1.0微米。睫状体中存在的P2X受体负责降低眼压。此外，在光线条件下，1.0微米的ATP会导致眼压降低大约50％，但当黑暗出现时，ATP浓度降至0.30微米，这种浓度几乎只能使眼压降低16％[2]。与NP（核心纤维）细胞（100μM）相比，在较低的ATP处理水平（20μM）下发现AF（环纤维）细胞中ECM（细胞外基质）积累明显增加，表明AF细胞对细胞外ATP更敏感[3]。
实验结果表明，在体内测试中，使用25毫克/千克的ATP治疗Wistar大鼠可以更有效地减轻贝伐单抗引起的肾脏毒性，比苯噻啶（4毫克/千克）更为有效。在大鼠的膀胱附近以1和5毫克/千克的剂量进行动脉内注射（i.a.），会迅速、节律性地增加膀胱压力，并在注射后立即排尿。
| Cas No. | 56-65-5 | SDF | |
| 别名 | 腺苷三磷酸; Adenosine 5'-triphosphate | ||
| Canonical SMILES | O[C@@H]([C@H]([C@H](N1C=NC2=C1N=CN=C2N)O3)O)[C@H]3COP(O)(OP(OP(O)(O)=O)(O)=O)=O | ||
| 分子式 | C10H16N5O13P3 | 分子量 | 507.18 |
| 溶解度 | Water : ≥ 100 mg/mL (197.17 mM) | 储存条件 | Store at 2-8°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.9717 mL | 9.8584 mL | 19.7169 mL |
| 5 mM | 0.3943 mL | 1.9717 mL | 3.9434 mL |
| 10 mM | 0.1972 mL | 0.9858 mL | 1.9717 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
ATP synthesis and storage
Purinergic Signal 2012 Sep;8(3):343-57.PMID:22528680DOI:10.1007/s11302-012-9305-8.
Since 1929, when it was discovered that ATP is a substrate for muscle contraction, the knowledge about this purine nucleotide has been greatly expanded. Many aspects of cell metabolism revolve around ATP production and consumption. It is important to understand the concepts of glucose and oxygen consumption in aerobic and anaerobic life and to link bioenergetics with the vast amount of reactions occurring within cells. ATP is universally seen as the energy exchange factor that connects anabolism and catabolism but also fuels processes such as motile contraction, phosphorylations, and active transport. It is also a signalling molecule in the purinergic signalling mechanisms. In this review, we will discuss all the main mechanisms of ATP production linked to ADP phosphorylation as well the regulation of these mechanisms during stress conditions and in connection with calcium signalling events. Recent advances regarding ATP storage and its special significance for purinergic signalling will also be reviewed.
Extracellular ATP: A Feasible Target for Cancer Therapy
Cells 2020 Nov 17;9(11):2496.PMID:33212982DOI:10.3390/cells9112496.
Adenosine triphosphate (ATP) is one of the main biochemical components of the tumor microenvironment (TME), where it can promote tumor progression or tumor suppression depending on its concentration and on the specific ecto-nucleotidases and receptors expressed by immune and cancer cells. ATP can be released from cells via both specific and nonspecific pathways. A non-regulated release occurs from dying and damaged cells, whereas active release involves exocytotic granules, plasma membrane-derived microvesicles, specific ATP-binding cassette (ABC) transporters and membrane channels (connexin hemichannels, pannexin 1 (PANX1), calcium homeostasis modulator 1 (CALHM1), volume-regulated anion channels (VRACs) and maxi-anion channels (MACs)). Extracellular ATP acts at P2 purinergic receptors, among which P2X7R is a key mediator of the final ATP-dependent biological effects. Over the years, P2 receptor- or ecto-nucleotidase-targeting for cancer therapy has been proposed and actively investigated, while comparatively fewer studies have explored the suitability of TME ATP as a target. In this review, we briefly summarize the available evidence suggesting that TME ATP has a central role in determining tumor fate and is, therefore, a suitable target for cancer therapy.
Imaging Adenosine Triphosphate (ATP)
Biol Bull 2016 Aug;231(1):73-84.PMID:27638696DOI:10.1086/689592.
Adenosine triphosphate (ATP) is a universal mediator of metabolism and signaling across unicellular and multicellular species. There is a fundamental interdependence between the dynamics of ATP and the physiology that occurs inside and outside the cell. Characterizing and understanding ATP dynamics provide valuable mechanistic insight into processes that range from neurotransmission to the chemotaxis of immune cells. Therefore, we require the methodology to interrogate both temporal and spatial components of ATP dynamics from the subcellular to the organismal levels in live specimens. Over the last several decades, a number of molecular probes that are specific to ATP have been developed. These probes have been combined with imaging approaches, particularly optical microscopy, to enable qualitative and quantitative detection of this critical molecule. In this review, we survey current examples of technologies available for visualizing ATP in living cells, and identify areas where new tools and approaches are needed to expand our capabilities.
ATP release during seizures - A critical evaluation of the evidence
Brain Res Bull 2019 Sep;151:65-73.PMID:30660718DOI:10.1016/j.brainresbull.2018.12.021.
That adenosine 5' triphosphate (ATP) functions as an extracellular signaling molecule has been established since the 1970s. Ubiquitous throughout the body as the principal molecular store of intracellular energy, ATP has a short extracellular half-life and is difficult to measure directly. Extracellular ATP concentrations are dependent both on the rate of cellular release and of enzymatic degradation. Some findings from in vitro studies suggest that extracellular ATP concentrations increase during high levels of neuronal activity and seizure-like events in hippocampal slices. Pharmacological studies suggest that antagonism of ATP-sensitive purinergic receptors can suppress the severity of seizures and block epileptogenesis. Directly measuring extracellular ATP concentrations in the brain, however, has a number of specific challenges, notably, the rapid hydrolysis of ATP and huge gradient between intracellular and extracellular compartments. Two studies using microdialysis found no change in extracellular ATP in the hippocampus of rats during experimentally-induced status epilepticus. One of which demonstrated that ATP increased measurably, only in the presence of ectoATPase inhibitors, with the other study demonstrating increases only during later spontaneous seizures. Current evidence is mixed and seems highly dependent on the model used and method of detection. More sensitive methods of detection with higher spatial resolution, which induce less tissue disruption will be necessary to provide evidence for or against the hypothesis of seizure-induced elevations in extracellular ATP. Here we describe the current hypothesis for ATP release during seizures and its role in epileptogenesis, describe the technical challenges involved and critically examine the current evidence.
ATP as a co-transmitter with noradrenaline in sympathetic nerves--function and fate
Ciba Found Symp 1996;198:223-35; discussion 235-8.PMID:8879828DOI:10.1002/9780470514900.ch13.
ATP and noradrenaline are co-stored in synaptic vesicles in sympathetic nerves and when co-released act postjunctionally to evoke contraction of visceral and vascular smooth muscle. In the original purinergic nerve hypothesis it was proposed that ATP would then be sequentially broken down to ADP, AMP and adenosine. Although such breakdown can be measured, it is not clear how the time-scale of breakdown compares with the time-course of the postjunctional actions of ATP. We have investigated the role of ectoATPase in modulating purinergic neurotransmission in the guinea-pig vas deferens using ARL67156 (formerly FPL67516), a recently developed inhibitor of ectoATPase. ARL67156 (1-100 microM) potentiated neurogenic contractions in a concentration-dependent manner. Onset of potentiation was rapid and the effect reversed rapidly on washout of the drug. The effect was also frequency dependent, being greater at lower frequencies. The purinergic component of the neurogenic contraction was isolated using the alpha 1 antagonist prazosin (100 nM) and ARL67156 caused a similar potentiation. ARL67156 also potentiated contractions evoked by exogenous ATP (100 microM), but had no effect on those of the stable analogue alpha, beta-methylene ATP (500 nM). In the presence of the P2 purinoceptor antagonist PPADS (100 microM), ARL67156 also had no effect on contractions evoked by noradrenaline (10 microM) or KCI (40 mM). These results are consistent with an inhibitory action of ARL67156 on ectoATPase and suggest that ectoATPase modulates purinergic transmission in the guinea-pig vas deferens. When released from sympathetic nerves, ATP acts at the P2X purinoceptor, a ligand-gated cation channel, to evoke depolarization and contraction. In single acutely dissociated smooth muscle cells of the rat tail artery, studied under voltage-clamp conditions, ATP and its analogues evoke an inward current, with a rank order potency of 2-methylthioATP = ATP > alpha, beta-methylene ATP. This is very different from the order of potency for evoking contraction in whole vessel rings, which is alpha, beta-methylene ATP > > 2-methylthioATP > or = ATP. This discrepancy can be explained by a previously unrecognized attenuation of the action of ATP and 2-methylthioATP, but not alpha, beta-methylene ATP, by ectoATPase in whole tissues.